@article{Cai2018,
title = {Road traffic noise, air pollution and incident cardiovascular disease: A joint analysis of the HUNT, EPIC-Oxford and UK Biobank cohorts},
author = {Yutong Cai and SusanHodgson and Marta Blangiardo and John Gulliver and David Morley and Daniela Fecht and DanielleVienneau and Kees de Hoogh and Tim Key and Kristian Hveem and Paul Elliott and Anna L.Hansell},
url = {https://www.sciencedirect.com/science/article/pii/S0160412017320548?via%3Dihub},
year = {2018},
date = {2018-03-05},
journal = {Environment International},
abstract = {This study aimed to investigate the effects of long-term exposure to road traffic noise and air pollution on incident cardiovascular disease (CVD) in three large cohorts: HUNT, EPIC-Oxford and UK Biobank.

Methods

In pooled complete-case sample of the three cohorts from Norway and the United Kingdom (N = 355,732), 21,081 incident all CVD cases including 5259 ischemic heart disease (IHD) and 2871 cerebrovascular cases were ascertained between baseline (1993–2010) and end of follow-up (2008–2013) through medical record linkage. Annual mean 24-hour weighted road traffic noise (Lden) and air pollution (particulate matter with aerodynamic diameter ≤ 10 μm [PM10], ≤2.5 μm [PM2.5] and nitrogen dioxide [NO2]) exposure at baseline address was modelled using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU) and European-wide Land Use Regression models. Individual-level covariate data were harmonised and physically pooled across the three cohorts. Analysis was via Cox proportional hazard model with mutual adjustments for both noise and air pollution and potential confounders.

Results

No significant associations were found between annual mean Lden and incident CVD, IHD or cerebrovascular disease in the overall population except that the association with incident IHD was significant among current-smokers. In the fully adjusted models including adjustment for Lden, an interquartile range (IQR) higher PM10 (4.1 μg/m3) or PM2.5 (1.4 μg/m3) was associated with a 5.8% (95%CI: 2.5%–9.3%) and 3.7% (95%CI: 0.2%–7.4%) higher risk for all incident CVD respectively. No significant associations were found between NO2 and any of the CVD outcomes.

This study aimed to investigate the effects of long-term exposure to road traffic noise and air pollution on incident cardiovascular disease (CVD) in three large cohorts: HUNT, EPIC-Oxford and UK Biobank.

Methods

In pooled complete-case sample of the three cohorts from Norway and the United Kingdom (N = 355,732), 21,081 incident all CVD cases including 5259 ischemic heart disease (IHD) and 2871 cerebrovascular cases were ascertained between baseline (1993–2010) and end of follow-up (2008–2013) through medical record linkage. Annual mean 24-hour weighted road traffic noise (Lden) and air pollution (particulate matter with aerodynamic diameter ≤ 10 μm [PM10], ≤2.5 μm [PM2.5] and nitrogen dioxide [NO2]) exposure at baseline address was modelled using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU) and European-wide Land Use Regression models. Individual-level covariate data were harmonised and physically pooled across the three cohorts. Analysis was via Cox proportional hazard model with mutual adjustments for both noise and air pollution and potential confounders.

Results

No significant associations were found between annual mean Lden and incident CVD, IHD or cerebrovascular disease in the overall population except that the association with incident IHD was significant among current-smokers. In the fully adjusted models including adjustment for Lden, an interquartile range (IQR) higher PM10 (4.1 μg/m3) or PM2.5 (1.4 μg/m3) was associated with a 5.8% (95%CI: 2.5%–9.3%) and 3.7% (95%CI: 0.2%–7.4%) higher risk for all incident CVD respectively. No significant associations were found between NO2 and any of the CVD outcomes.

Conclusions

We found suggestive evidence of a possible association between road traffic noise and incident IHD, consistent with current literature. Long-term particulate air pollution exposure, even at concentrations below current European air quality standards, was significantly associated with incident CVD.

@article{Cai2017,
title = {Ambient air pollution, traffic noise and adult asthma prevalence: a BioSHaRE approach},
author = {Yutong Cai and Wilma L. Zijlema and Dany Doiron and Marta Blangiardo and Paul R. Burton and Isabel Fortier and Amadou Gaye and John Gulliver and Kees de Hoogh and Kristian Hveem and Stéphane Mbatchou and David W. Morley and Ronald P. Stolk and Paul Elliott and Anna L. Hansell and Susan Hodgson},
url = {http://erj.ersjournals.com/content/early/2016/10/20/13993003.02127-2015},
year = {2017},
date = {2017-11-01},
journal = {European Respiratory Journal 2016},
abstract = {We investigated the effects of both ambient air pollution and traffic noise on adult asthma prevalence, using harmonised data from three European cohort studies established in 2006–2013 (HUNT3, Lifelines and UK Biobank).

Residential exposures to ambient air pollution (particulate matter with aerodynamic diameter ≤10 µm (PM10) and nitrogen dioxide (NO2)) were estimated by a pan-European Land Use Regression model for 2007. Traffic noise for 2009 was modelled at home addresses by adapting a standardised noise assessment framework (CNOSSOS-EU). A cross-sectional analysis of 646 731 participants aged ≥20 years was undertaken using DataSHIELD to pool data for individual-level analysis via a “compute to the data” approach. Multivariate logistic regression models were fitted to assess the effects of each exposure on lifetime and current asthma prevalence.

PM10 or NO2 higher by 10 µg·m−3 was associated with 12.8% (95% CI 9.5–16.3%) and 1.9% (95% CI 1.1–2.8%) higher lifetime asthma prevalence, respectively, independent of confounders. Effects were larger in those aged ≥50 years, ever-smokers and less educated. Noise exposure was not significantly associated with asthma prevalence.

This study suggests that long-term ambient PM10 exposure is associated with asthma prevalence in western European adults. Traffic noise is not associated with asthma prevalence, but its potential to impact on asthma exacerbations needs further investigation.},
keywords = {5179, air pollution, asthma, featured},
pubstate = {published},
tppubtype = {article}
}

We investigated the effects of both ambient air pollution and traffic noise on adult asthma prevalence, using harmonised data from three European cohort studies established in 2006–2013 (HUNT3, Lifelines and UK Biobank).

Residential exposures to ambient air pollution (particulate matter with aerodynamic diameter ≤10 µm (PM10) and nitrogen dioxide (NO2)) were estimated by a pan-European Land Use Regression model for 2007. Traffic noise for 2009 was modelled at home addresses by adapting a standardised noise assessment framework (CNOSSOS-EU). A cross-sectional analysis of 646 731 participants aged ≥20 years was undertaken using DataSHIELD to pool data for individual-level analysis via a “compute to the data” approach. Multivariate logistic regression models were fitted to assess the effects of each exposure on lifetime and current asthma prevalence.

PM10 or NO2 higher by 10 µg·m−3 was associated with 12.8% (95% CI 9.5–16.3%) and 1.9% (95% CI 1.1–2.8%) higher lifetime asthma prevalence, respectively, independent of confounders. Effects were larger in those aged ≥50 years, ever-smokers and less educated. Noise exposure was not significantly associated with asthma prevalence.

This study suggests that long-term ambient PM10 exposure is associated with asthma prevalence in western European adults. Traffic noise is not associated with asthma prevalence, but its potential to impact on asthma exacerbations needs further investigation.